The atypical cell cycle regulator Spy1 suppresses differentiation of the neuroblastoma stem cell population
Dorota Lubanska1 and Lisa A. Porter1
1 Department of Biological Sciences University of Windsor OntarioWindsor, ON
Lisa A. Porter, email:
Keywords: Spdya, RINGO, Cdk, Cyclin, neurogenesis
Received: April 4, 2014 Accepted: May 4, 2014 Published: May 6, 2014
Neuroblastoma is an aggressive pediatric cancer originating embryonically from the neural crest. The heterogeneity of the disease, as most solid tumors, complicates diagnosis and treatment. In neuroblastoma this heterogeneity is well represented in both primary tumours and derived cell lines and has been shown to be driven by a population of stem-like tumour initiating cells. Resolving the molecular mediators driving the division of this population of cells may indicate effective therapeutic options for neuroblastoma patients. This study has determined that the atypical cyclin-like protein Spy1, recently indicated in driving symmetric division of glioma stem cells, is a critical factor in the stem-like properties of neuroblastoma tumor initiating cell populations. Spy1 activates Cyclin Dependent Kinases (CDK) in a manner that is unique from classical cyclins. Hence this discovery may represent an important opportunity to design CDK inhibitor drugs to uniquely target subpopulations of cells within these aggressive neural tumours.